Calcium/calmodulin-dependent protein kinase type II (CamKII) is a ubiquitous brain enzyme implicated in a wide variety of neuronal processes. Understanding CamKII has become increasingly complicated with the recent identification of multiple gene transcripts coding for separate subunits. Previous studies have shown that mRNA for the alpha subunit of CamKII can be increased by reduction of afferent input. In this study we have examined the regulation of αCamKII mRNA following increased activity due to seizures. Using in situ hybridization with a cRNA probe against the rat αCamKII sequence we found reduced levels of hybridization following limbic seizures induced by lesions of the hilus of the dentate gyrus. Hybridization was most dramatically reduced in the granule cells of the dentate gyrus and the pyramidal cells of hippocampal region CA1 There were also significant reductions in hybridization in the superficial layers of neocortex and piriform cortex. In each of these regions hybridization was decreased in the molecular layers which is consistent with the reported dendritic localization of αCamKII mRNA. All changes in mRNA content were transient, with maximal reductions at 24 h following lesion placement and a return to control levels by 96 h. These findings demonstrate the negative regulation of αCamKII mRNA by seizure activity and raise the possibility that synthesis of this kinase may be regulated by normal physiological activity.
- Activity-dependent regulation
- Hilus lesion
- Protein kinase
ASJC Scopus subject areas
- Molecular Biology
- Cellular and Molecular Neuroscience